Anti-SF3B1 antibody [EPR11987(B)]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

SF3B1 also known as Splicing Factor 3B subunit 1 plays an important role in the mRNA splicing process. This protein participates in the splicing machinery as part of the spliceosome contributing to the removal of introns from pre-mRNA. SF3B1 has a molecular weight of approximately 160 kDa. It is ubiquitously expressed yet shows a high level of activity in tissues with rapid cell division such as the bone marrow and lymphatic tissue reflecting its central involvement in gene expression regulation.

Biological function summary

SF3B1 is an essential component of the spliceosomal complex specifically the U2 snRNP component. It helps establish the branchpoint recognition complex ensuring accurate RNA splicing necessary for producing functional mRNA molecules. This process is important for the expression of diverse protein-coding genes affecting multiple aspects of cellular function and identity. The protein interacts with other spliceosomal proteins like SF3A and U2AF to guide the precise removal of non-coding sequences enabling proper translation into proteins.

Pathways

SF3B1 is involved in the mRNA processing pathway and influences the cell cycle pathway. During mRNA processing SF3B1 aids in assembling the spliceosome facilitating the excision of introns. The protein interacts with components like SF3B2 in coordinating splicing with other RNA processing events. In the cell cycle pathway SF3B1 indirectly affects gene expression and stability influencing cell cycle progression and serving as a regulatory node by modulating the splicing of key regulators active during cell division.

Associated diseases and disorders

Several studies associate SF3B1 mutations with certain types of cancer including myelodysplastic syndrome and chronic lymphocytic leukemia. These mutations often result in aberrant splicing events leading to altered gene expression profiles that can promote tumorigenesis. Within these disease contexts SF3B1 abnormalities can influence interactions with related proteins like SRSF2 contributing to misregulated splicing patterns of genes that drive cancerous transformations and affect patient prognosis.